Rheumatic fever is caused by the body’s immunological reaction to a Streptococcus pyogenes throat infection. Rheumatic heart disease is the long-term cardiac damage induced by a single severe or recurring episode of rheumatic fever.
This illness primarily affects people in low- and middle-income countries and indigenous peoples in affluent countries when initial S. pyogenes infections are not treated, allowing for the development of dangerous post-infectious sequelae.
Epidemiology
Rheumatic fever incidence rates among indigenous communities in Australia and North Queensland have been estimated to be as significant as 155 per 100,000 children between 5-14 years, with the incidence in the Northern Territory reported to be 380 per 100,000 children in 2002.
Rheumatic fever mostly affects adolescents and children aged 4 to 19, who are generally Pasifika and Maori ethnicity and live in poor socioeconomic zones of the North Island.
It should also be highlighted that these incidence and prevalence numbers are likely to be understated due to fluctuating and limited data collecting in resource-poor countries, where Rheumatic fever and Rheumatic heart disease rates are generally greatest.
Anatomy
Pathophysiology
The immune system is activated by a pharyngeal infection, which results in the transmission of S. pyogenes antigens to B and T cells. CD4+ T cells are stimulated, and B cells produce specific IgG and IgM antibodies.
Tissue damage is caused by an immune-mediated pathway that begins with molecular imitation. Because of the resemblance between the infectious agent and human proteins, antibodies and/or T cells directed against human proteins are cross activated.
This cross-reactive immune response causes rheumatic fever-like clinical features such as carditis because of antibody binding and T cell infiltration; temporary arthritis due to immune complex formation; chorea due to antibody binding to basal ganglia; and appearances on skin because of delayed hypersensitivity reaction.
Etiology
Age, gender, and multiple environmental variables are the risk factors. It primarily affects children aged 5 to 14 years, while first occurrences can affect children as young as five years old. Recurrent episodes are more common in older children and can last into young adulthood. Since Rheumatic heart disease is generally the consequence of accumulated damage, the greatest prevalence occurs in the twenties or thirties of a patient.
However, the incidence in adolescents and children remains significant. Environmental variables increase exposure to S. pyogenes infections, which increases the occurrence of rheumatic fever. Residential crowding, which favors the transmission of S. pyogenes infections, is a primary environmental factor that raises the incidence.
Furthermore, Rheumatic fever has been proven to be more widespread in rural and isolated places, as well as metropolitan slums; however, this is likely due to other risk factors, such as increased household congestion due to poor socioeconomic levels or restricted access to medical services.
Rheumatic fever is caused by the body’s immunological reaction to a Streptococcus pyogenes throat infection. Rheumatic heart disease is the long-term cardiac damage induced by a single severe or recurring episode of rheumatic fever.
This illness primarily affects people in low- and middle-income countries and indigenous peoples in affluent countries when initial S. pyogenes infections are not treated, allowing for the development of dangerous post-infectious sequelae.
Rheumatic fever incidence rates among indigenous communities in Australia and North Queensland have been estimated to be as significant as 155 per 100,000 children between 5-14 years, with the incidence in the Northern Territory reported to be 380 per 100,000 children in 2002.
Rheumatic fever mostly affects adolescents and children aged 4 to 19, who are generally Pasifika and Maori ethnicity and live in poor socioeconomic zones of the North Island.
It should also be highlighted that these incidence and prevalence numbers are likely to be understated due to fluctuating and limited data collecting in resource-poor countries, where Rheumatic fever and Rheumatic heart disease rates are generally greatest.
The immune system is activated by a pharyngeal infection, which results in the transmission of S. pyogenes antigens to B and T cells. CD4+ T cells are stimulated, and B cells produce specific IgG and IgM antibodies.
Tissue damage is caused by an immune-mediated pathway that begins with molecular imitation. Because of the resemblance between the infectious agent and human proteins, antibodies and/or T cells directed against human proteins are cross activated.
This cross-reactive immune response causes rheumatic fever-like clinical features such as carditis because of antibody binding and T cell infiltration; temporary arthritis due to immune complex formation; chorea due to antibody binding to basal ganglia; and appearances on skin because of delayed hypersensitivity reaction.
Age, gender, and multiple environmental variables are the risk factors. It primarily affects children aged 5 to 14 years, while first occurrences can affect children as young as five years old. Recurrent episodes are more common in older children and can last into young adulthood. Since Rheumatic heart disease is generally the consequence of accumulated damage, the greatest prevalence occurs in the twenties or thirties of a patient.
However, the incidence in adolescents and children remains significant. Environmental variables increase exposure to S. pyogenes infections, which increases the occurrence of rheumatic fever. Residential crowding, which favors the transmission of S. pyogenes infections, is a primary environmental factor that raises the incidence.
Furthermore, Rheumatic fever has been proven to be more widespread in rural and isolated places, as well as metropolitan slums; however, this is likely due to other risk factors, such as increased household congestion due to poor socioeconomic levels or restricted access to medical services.
1.2 million units given IM once a month or 600000 units given IM for every 2 weeks.
https://www.ncbi.nlm.nih.gov/books/NBK425394/
medtigo
Rheumatic fever
Updated :
October 10, 2022
Rheumatic fever is caused by the body’s immunological reaction to a Streptococcus pyogenes throat infection. Rheumatic heart disease is the long-term cardiac damage induced by a single severe or recurring episode of rheumatic fever.
This illness primarily affects people in low- and middle-income countries and indigenous peoples in affluent countries when initial S. pyogenes infections are not treated, allowing for the development of dangerous post-infectious sequelae.
Rheumatic fever incidence rates among indigenous communities in Australia and North Queensland have been estimated to be as significant as 155 per 100,000 children between 5-14 years, with the incidence in the Northern Territory reported to be 380 per 100,000 children in 2002.
Rheumatic fever mostly affects adolescents and children aged 4 to 19, who are generally Pasifika and Maori ethnicity and live in poor socioeconomic zones of the North Island.
It should also be highlighted that these incidence and prevalence numbers are likely to be understated due to fluctuating and limited data collecting in resource-poor countries, where Rheumatic fever and Rheumatic heart disease rates are generally greatest.
The immune system is activated by a pharyngeal infection, which results in the transmission of S. pyogenes antigens to B and T cells. CD4+ T cells are stimulated, and B cells produce specific IgG and IgM antibodies.
Tissue damage is caused by an immune-mediated pathway that begins with molecular imitation. Because of the resemblance between the infectious agent and human proteins, antibodies and/or T cells directed against human proteins are cross activated.
This cross-reactive immune response causes rheumatic fever-like clinical features such as carditis because of antibody binding and T cell infiltration; temporary arthritis due to immune complex formation; chorea due to antibody binding to basal ganglia; and appearances on skin because of delayed hypersensitivity reaction.
Age, gender, and multiple environmental variables are the risk factors. It primarily affects children aged 5 to 14 years, while first occurrences can affect children as young as five years old. Recurrent episodes are more common in older children and can last into young adulthood. Since Rheumatic heart disease is generally the consequence of accumulated damage, the greatest prevalence occurs in the twenties or thirties of a patient.
However, the incidence in adolescents and children remains significant. Environmental variables increase exposure to S. pyogenes infections, which increases the occurrence of rheumatic fever. Residential crowding, which favors the transmission of S. pyogenes infections, is a primary environmental factor that raises the incidence.
Furthermore, Rheumatic fever has been proven to be more widespread in rural and isolated places, as well as metropolitan slums; however, this is likely due to other risk factors, such as increased household congestion due to poor socioeconomic levels or restricted access to medical services.
https://www.ncbi.nlm.nih.gov/books/NBK425394/
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